Cilostazol 100mg tablets
Requires a prescription from a doctor or prescriber
Cilostazol is a quinolinone derivative and antiplatelet agent with vasodilating properties that has been used in the symptomatic treatment of intermittent claudication in patients with peripheral ischaemia.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
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Drug safety updates
MHRA alerts for Cilostazol
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Cilostazol
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Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Cilostazol
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
18 branded products available
MHRA licensed products
View all licensed products for Cilostazol on the MHRA register
Pletal 100mg tablets
Pletal 100mg tablets
Cilostazol 100mg tablets
Cilostazol 100mg tablets
Cilostazol 100mg tablets
Cilostazol 100mg tablets
Cilostazol 100mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
200 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Cilostazol, naftidrofuryl oxalate, pentoxifylline and inositol nicotinate for the treatment of intermittent claudication in people with peripheral arterial disease (TA223)
Peripheral arterial disease: diagnosis and management (CG147)
Spiral Flow peripheral vascular graft for treating peripheral arterial disease (MIB34)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 20 · Randomised trials: 28 · 1997–2026
Showing the 50 most relevant studies, sorted by most relevant.
Paul D Thompson, Richard Zimet, William P Forbes, et al.
The American Journal of Cardiology, 2002
J. Wardlaw, L. Woodhouse, I. Mhlanga, et al.
JAMA Neurology, 2023
Judith G. Regensteiner, John E. Ware, Walter J. McCarthy, et al.
Journal of the American Geriatrics Society, 2002
Caroline A. McHutchison, Gordon W. Blair, J. Appleton, et al.
Stroke, 2020
K. Toyoda, S. Uchiyama, T. Yamaguchi, et al.
The Lancet. Neurology, 2019
Aidin Abedi, S. Sizdahkhani, W. Choi, et al.
Neurosurgical focus, 2023
Sun J, Wang D, Zhao Y, et al.
2025
- Carotid Arteries
- Carotid Stenosis
- Graft Occlusion, Vascular
ObjectivesThere is some controversy regarding drug therapy to prevent in-stent restenosis (ISR) after carotid artery stenting. In recent years, cilostazol has received increasing research attention. We performed a meta-analysis to evaluate the effects of cilostazol on the outcome of ISR after carotid stenting.MethodsA meta-analysis was carried out to identify the clinical trials that had been published up to 22 December 2024. The databases PubMed, Embase, Cochrane Library, CNKI and Wanfang have all been queried. The study population was composed of patients with stent carotid heart disease who were receiving cilostazol. Results included in-stent-restenosis, ischemic stroke and all-cause mortality. Publications were reviewed according to the Cochrane Handbook and the guidelines set out in the Preferred Reporting Project for Systematic Review and Meta-Analysis (PRISMA 2020). The methodological quality of the studies was assessed using the Revised Cochrane Risk of Bias tool for randomized trials (RoB 2.0) and the Risk of Bias in Non-Randomized Studies of Interventions (ROBINS-I).ResultsThis study was registered with INPLASY (number INPLASY202510004). A total of 1975 patients were included in 4 randomized controlled trials (RCTs) and 5 non-RCTs. A statistically significant reduction in ISR was observed for antiplatelet regimens including cilostazol compared to the control group (OR = 0.27, 95%CI: 0.13 ~ 0.54, P2 = 30%). Subgroup analysis revealed this finding was primarily driven by non-randomized controlled trials (non-RCTs), demonstrating a consistent effect (OR = 0.17, 95%CI: 0.08 ~ 0.39, P2 = 0%). For other primary end events, no significant differences were noted in the incidence of ischemic stroke (OR = 0.83, 95%CI: 0.50 ~ 1.39, P = 0.49, I2 = 0%) or all cause death (OR = 0.53, 95%CI: 0.26 ~ 1.05, P = 0.07, I2 = 0%). The certainty of evidence for the ISR outcome was rated as low.ConclusionsCilostazol was associated with less postoperative carotid stent restenosis, with no statistically significant difference in ischemic stroke and all-cause mortality.
Abstract licence: CC BY-NC-ND
Bruun CF, Fredskild MU, Faurholt-Jepsen M, et al.
2026
- Aspirin
- Dipyridamole
- Fibrinolytic Agents
Evidence suggests shared pathophysiologic mechanisms between severe mental illness (SMI) and cardiovascular disease (CVD). Drugs used for CVD, such as antithrombotic agents (ATAs), may therefore be repurposed for the treatment of SMI. We conducted the first systematic review and meta-analysis (PROSPERO registration CRD42024524420) of ATAs for SMI and reported results according to PRISMA guidelines. We searched MEDLINE, Embase, and PsycINFO (October 10, 2024) and performed random-effects meta-analysis. Risk of bias was assessed using the Cochrane Risk of Bias 2 tool, and the certainty of evidence was evaluated using the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) framework. Primary outcomes were symptom severity, risk of recurrence, and tolerability. We included 12 randomized trials investigating aspirin, cilostazol, and dipyridamole in a total of 742 patients with schizophrenia, major depression, and bipolar disorder. Results showed that ATA treatment may reduce depressive symptoms in patients with SMI (SMD -0.62; 95 % CI -1.11 to -0.13; 8 studies; very low-certainty evidence). Based on studies with low risk of bias, ATA treatment may reduce PANSS total score compared with placebo (SMD -0.57; 95 % CI -0.86 to -0.28; 3 studies; very low-certainty evidence). Tolerability of ATAs may not differ from placebo (RR 0.89; 95 % CI 0.57-1.40; 9 studies; very low-certainty evidence). Given the low certainty of the evidence, effect estimates should be interpreted with caution. The therapeutic potential of ATAs in SMI remains uncertain. Well-powered RCTs investigating clinically relevant outcomes in clearly defined populations are needed.
Abstract licence: CC BY-NC-ND
Hosna Elshony, Mohammed Ezzat Elwan, Ibraheim Al-Ahmer, et al.
The Egyptian Journal of Neurology, Psychiatry and Neurosurgery, 2025
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
32 found
Half-life
11-13 hours
Mechanism
Cilostazol and several of its metabolites are cyclic AMP (cAMP) phosphodiesteras…
Food interactions
2 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
90%
Half-life
11-13 hours
Protein binding
95-98%
Metabolism
50%
Elimination
74%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1906 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
No measurable amount of unchanged cilostazol was excreted in the urine, and less than 2% of the dose was excreted as 3,4-dehydro-cilostazol.
About 30% of the dose was excreted in urine as 4'-trans-hydroxy-cilostazol.
Proteins and enzymes this drug interacts with in the body
PMID:1315035 PMID:25961942 PMID:8155697 PMID:8695850
Also has activity toward cUMP .
PMID:27975297
Independently of its catalytic activity it is part of an E2/17beta-estradiol-induced pro-apoptotic signaling pathway. E2 stabilizes the PDE3A/SLFN12 complex in the cytosol, promoting the dephosphorylation of SLFN12 and activating its pro-apoptotic ribosomal RNA/rRNA ribonuclease activity. This apoptotic pathway might be relevant in tissues with high concentration of E2 and be for instance involved in placenta remodeling PMID:31420216 PMID:34707099
Enzymes involved in drug metabolism — important for understanding drug interactions
Involved compounds
ATC B01AC23
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Cilostazol
Additional database identifiers
ChemSpider
2652
BindingDB
50225508
ZINC
ZINC000001552174
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8778
GenAtlas
PDE3A
GeneCards
PDE3A
GenBank Gene Database
M91667
GenBank Protein Database
38201493
Guide to Pharmacology
1298
UniProt Accession
PDE3A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72